NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic Fibroblasts

Cholesterol, its derivatives, and metabolites from its biosynthesis are important components of the cell and play an essential role in many intracellular processes, including cell signaling, regulation of the cell cycle, etc. In this paper, it has been shown that depletion of the cholesterol biosynt...

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Main Authors: L.R. Gabitova, I.A. Astsaturov
Format: Article
Language:English
Published: Kazan Federal University 2015-03-01
Series:Учёные записки Казанского университета: Серия Естественные науки
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Online Access:http://kpfu.ru/portal/docs/F_1335647387/157_1_est_10_e.pdf
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author L.R. Gabitova
I.A. Astsaturov
author_facet L.R. Gabitova
I.A. Astsaturov
author_sort L.R. Gabitova
collection DOAJ
description Cholesterol, its derivatives, and metabolites from its biosynthesis are important components of the cell and play an essential role in many intracellular processes, including cell signaling, regulation of the cell cycle, etc. In this paper, it has been shown that depletion of the cholesterol biosynthesis pathway enzyme NSDHL (NAD(P)H-dependent steroid dehydrogenase-like) and accumulation of its metabolites lead to an increased rate of cellular senescence and reduction of proliferation in mouse embryonic fibroblasts. The phenomenon described can be useful for developing new strategies of targeting cholesterol biosynthesis pathway in cancer cells in order to increase their senescence and inhibit proliferation.
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issn 1815-6169
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publishDate 2015-03-01
publisher Kazan Federal University
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series Учёные записки Казанского университета: Серия Естественные науки
spelling doaj-art-85ecfd8f872b45d08e027b18b0deefa92025-08-20T02:43:06ZengKazan Federal UniversityУчёные записки Казанского университета: Серия Естественные науки1815-61692500-218X2015-03-011571127139NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic FibroblastsL.R. Gabitova0I.A. Astsaturov1Kazan Federal University, Kazan, 420008 Russia; Fox Chase Cancer Center, Philadelphia, PA 19111, USAKazan Federal University, Kazan, 420008 Russia; Fox Chase Cancer Center, Philadelphia, PA 19111, USACholesterol, its derivatives, and metabolites from its biosynthesis are important components of the cell and play an essential role in many intracellular processes, including cell signaling, regulation of the cell cycle, etc. In this paper, it has been shown that depletion of the cholesterol biosynthesis pathway enzyme NSDHL (NAD(P)H-dependent steroid dehydrogenase-like) and accumulation of its metabolites lead to an increased rate of cellular senescence and reduction of proliferation in mouse embryonic fibroblasts. The phenomenon described can be useful for developing new strategies of targeting cholesterol biosynthesis pathway in cancer cells in order to increase their senescence and inhibit proliferation.http://kpfu.ru/portal/docs/F_1335647387/157_1_est_10_e.pdfcholesterolcholesterol biosynthesis pathway metabolitesNAD(P)Н-dependent steroid dehydrogenase-likecellular senescenceinhibition of proliferation
spellingShingle L.R. Gabitova
I.A. Astsaturov
NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic Fibroblasts
Учёные записки Казанского университета: Серия Естественные науки
cholesterol
cholesterol biosynthesis pathway metabolites
NAD(P)Н-dependent steroid dehydrogenase-like
cellular senescence
inhibition of proliferation
title NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic Fibroblasts
title_full NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic Fibroblasts
title_fullStr NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic Fibroblasts
title_full_unstemmed NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic Fibroblasts
title_short NSDHL Depletion Promotes Cellular Senescence in Mouse Embryonic Fibroblasts
title_sort nsdhl depletion promotes cellular senescence in mouse embryonic fibroblasts
topic cholesterol
cholesterol biosynthesis pathway metabolites
NAD(P)Н-dependent steroid dehydrogenase-like
cellular senescence
inhibition of proliferation
url http://kpfu.ru/portal/docs/F_1335647387/157_1_est_10_e.pdf
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